While BPI may very well prove beneficial for some indications, the synopsis below illustrates why I am skeptical of some of the claims made by posters on this board:
Why may antibiotic therapy not be effective in resolving late
stages of sepsis syndrome?
Use of antibiotic therapy implies that the instigator of the septic cascade, a microorganism, continues to
mediate progression of the disease state. If the patient is in the late stages of sepsis syndrome, e.g.,
multiple organ dysfunction syndrome, this may not necessarily be the case. Infection by the
microorganism may have been resolved by the patient's immune system.
The pathogenesis of sepsis syndrome is a complex cascade of events that involves many mediators.
The factor instigating the cascade may be the release of endotoxin into the circulation from
gram-negative bacteria or a comparable, cell-wall substance from gram-positive bacteria or fungi.
Progression of the cascade may then be mediated by stimulation of non-specific and specific immune
system components, such as cytokines (tumor necrosis factor, the interleukins, platelet activating
factor), eicosanoids, complement components, and/or kinins.
Once the cascade begins, the clinical progression of disease can eventually become self-perpetuating,
independent of the original inflammatory trigger and/or mediators generated. Therefore, treatment
targeting a specific mediator, e.g., antibiotics or antibodies to TNF, is only effective if that mediator still
plays an active role in the progression of the patient's clinical condition.
Antimicrobial agents are most beneficial in treating the early clinical stages of sepsis syndrome, before
host factor mediators have had the opportunity to cause further progression down the septic cascade.
Source: Sundaresan R, Sheagren JN: Current understanding and treatment of sepsis. Infect Med
12(6):21-268, 274, 1995.
Tod |
